Using the yeast Saccharomyces we are examining the importance of DNA repair in normal meiosis and following exposure to DNA damaging agents during meiosis. Mutants in the three genetically defined UV and X-ray repair pathways are being used: rad 1 (excision repair), rad 52 (X-ray repair) and rad 6 (mutational repair). The rad 6 and rad 52 mutants do not prevent a normal round of meiotic DNA synthesis; however, recombination is abolished. No meiotic spore products are formed in rad 6 strains, whereas with rad 52 the spores are inviable. The rad 52 strains accumulate single-strand breaks or gaps in parental DNA during meiosis, whereas in RAD plus there is a transitory appearance of breaks. We conclude that the RAD 52 gene product which is required for normal meiosis is involved with recombination and the breaks may be intermediate in this process. Further experiments are underway to test this. We are also probing UV-induced mutations and postreplication processes during meiosis and comparing them to their mitotic counterpart using excision-defective strains. These studies will enable us to determine if there are repair mechanisms unique to meiosis and the effectiveness of mutagenic agents administered during meiosis.